Farah Vera M A, Joaquim Luis F, Morris Mariana
Boonshoft School of Medicine, Wright State University, Department of Pharmacology and Toxicology, Dayton, OH 45401, United States.
Physiol Behav. 2006 Nov 30;89(4):569-75. doi: 10.1016/j.physbeh.2006.07.015. Epub 2006 Sep 7.
Studies evaluated the role of the autonomic nervous system in the cardiovascular response to stress using radiotelemetric blood pressure (BP) recording coupled with autoregressive spectral analysis. Conscious male C57/BL6 mice with carotid arterial telemetric catheters were exposed to acute episodes of shaker stress before and after administration of cholinergic, beta1-adrenergic and alpha1-adrenergic receptor antagonists. Pulse interval (PI) and systolic arterial pressure (SAP) were analyzed for variance and the low frequency (LF: 0.1-1.0 Hz) and high frequency (HF: 1-5 Hz) spectral components. Stress (5 min) increased BP and heart rate (HR) as well as PI and SAP variability. PI variance increased from 41+/-6 to 75+/-14 ms2 while SAP variance increased from 25+/-5 to 55+/-9 mm Hg2. Autonomic blockade had specific effects on stress-induced changes in PI and SAP and their respective variability. Atropine reduced the tachycardia and abolished the increase in PI variance and its LF component. Data documents that in mice the cholinergic system is fundamental for the maintenance of HR variability. Atropine had no effects on the BP responses, either the increase in SAP or the variance associated with stress. Atenolol blocked the increase in PI and SAP variability induced by stress. Prazosin reduced the tachycardia produced by stress and blocked the increase in PI (only LF) and SAP variability. Using quantitative spectral analysis of telemetrically collected BP data in mice along with pharmacological antagonism, we were able to accurately determine the role of autonomic input in the mediation of the stress response. Data verify the role of sympathetic/parasympathetic balance in stress-induced changes in HR, BP and indices of variance.
研究使用无线电遥测血压（BP）记录结合自回归谱分析，评估了自主神经系统在心血管应激反应中的作用。将带有颈动脉遥测导管的清醒雄性C57/BL6小鼠在给予胆碱能、β1-肾上腺素能和α1-肾上腺素能受体拮抗剂之前和之后暴露于摇晃应激的急性发作中。分析脉搏间期（PI）和收缩期动脉压（SAP）的方差以及低频（LF：0.1 - 1.0 Hz）和高频（HF：1 - 5 Hz）谱成分。应激（5分钟）增加了血压和心率（HR）以及PI和SAP的变异性。PI方差从41±6增加到75±14 ms²，而SAP方差从25±5增加到55±9 mmHg²。自主神经阻滞对应激诱导的PI和SAP变化及其各自的变异性有特定影响。阿托品减少了心动过速并消除了PI方差及其LF成分的增加。数据表明，在小鼠中胆碱能系统对于维持HR变异性至关重要。阿托品对血压反应没有影响，无论是SAP的增加还是与应激相关的方差。阿替洛尔阻断了应激诱导的PI和SAP变异性的增加。哌唑嗪减少了应激产生的心动过速并阻断了PI（仅LF）和SAP变异性的增加。通过对小鼠遥测收集的BP数据进行定量谱分析以及药理学拮抗作用，我们能够准确确定自主神经输入在应激反应介导中的作用。数据验证了交感/副交感平衡在应激诱导的HR、BP和方差指数变化中的作用。
